This application proposes a scientific meeting on glucose-6-phosphate dehydrogenase (G6PD). Since the association of X-linked G6PD deficiency in red cells with chronic and drug/food-induced hemolytic anemia was found in mid-1950, both clinical and basic studies of this problem were greatly advanced. G6PD variation is the most prevalent and and heterogeneous human enzyme abnormality, and the major cause of hemolytic problems. The underlying mechanism of hemolysis due to G6PD deficiency, and kinetic and structural abnormalities of variant human G6PDs were extensively studied. Specific molecular abnormalities were defined in several G6PD variants. The hypothesis of "X-inactivation" was first proposed based on heterogeneity of heterozygous female red cells. G6PD became an important gene marker and tool for the study of X-inactivation, pathogenesis, aging and development, and several important discoveries were made in this field. Our knowledge of structure, function, hormonal and developmental control of G6PD and Hexose-6-phosphate dehydrogenase (H6PD) in non-human organisms were also advanced. Studies of the molecular biology of G6PD were extended in recent years, i.e. complete structure of normal human G6PD was determined and cDNA was cloned. The symposium proposed aims to define our current status of knowledge of: a) relationships of clinical manifestations of hemolytic anemia, red cell metabolism, and G6PD deficiency; b) G6PD variations and frequencies in various populations; c) structure, function and molecular biology of G6PD and G6PD locus; d) structural and functional abnormalities of G6PD variants; e) X-inactivation and pathogenesis studies using G6PD as a marker; and f) structure and function of G6PD in non-human organisms, hormonal and nutritional regulation, and evolution of G6PD and H6PD.